OBJECTIVE To provide a reference for pharmaceutical care in patients with ulcerative colitis （UC） and ankylosing spondylitis （AS） who developed pustular psoriasis induced by infliximab. METHODS Clinical pharmacists participated in the pharmaceutical care process of a patient with UC and AS who developed pustular psoriasis after using infliximab. The clinical pharmacists determined， using Naranjo’s Scale， that the correlation between the patient’s pustular psoriasis and infliximab was “likely”. Regarding the patient’s development of pustular psoriasis after using infliximab， the clinical pharmacists recommended discontinuing infliximab and switching to Upadacitinib extended-release tablets. For the patient’s skin allergic reaction after using upadacitinib， the clinical pharmacists advised continuing the use of upadacitinib and closely monitoring any potential adverse reactions during the treatment period. RESULTS The clinicians adopted the clinical pharmacists’ recommendation. Following the treatment， the patient’s symptoms were significantly alleviated， and the patient was discharged with medication. The follow-up after discharge showed that the treatment was effective and well-tolerated. CONCLUSIONS The clinical pharmacists analyzed the causal relationship between infliximab and pustular psoriasis. Through pharmaceutical care measures such as dynamic monitoring of skin lesions， evaluation of treatment responses， and optimization of drug regimens， they assisted the physicians in formulating an individualized medication plan， ensuring the safety and efficacy of the patient’s medication use.

Objective:To analyze the time point when patients with fatty liver disease had a significantly higher risk of elevated fasting blood glucose than those without in the physical examination group in Karamay Central Hospital, factors affecting the incidence of elevated blood glucose in patients with fatty liver disease, and the influence of the number of influencing factors on it.Methods:Physical examination data from Karamay Central Hospital during September 2008 to April 2017 were retrospectively analyzed. Combined with the survival analysis, the 1-,3-, 5-, and 7-year prevalence rates of elevated fasting glucose occurs in people with and without fatty liver disease were analyzed. Z-test was used to compare the survival rate difference at each time point. Cox regression model was used for multivariate analysis.Results:10 802 people were in the fatty liver group. The elevated fasting blood glucose incidence density was 61/1 000 person-years, and the 1-, 3-, 5-, and 7-year prevalence rates were 2%, 16%, 28%, and 38%, respectively. 29 579 people were in the non-fatty liver group. The elevated fasting blood glucose incidence density was 23/1000 person-years, and the 1-, 3-, 5-, and 7-year prevalence rates were 1%, 7%, 11%, and 16%, respectively. The short-term and long-term elevated fasting blood glucose incidence risk were significantly higher in fatty liver group than non-fatty liver group( P < 0.001). The elevated fasting blood glucose incidence risk was apparently higher in fatty liver group than that of non-fatty liver group from the first year onward ( P < 0.001). Age≥50 year’s old ( HR = 1.954, 95% CI :1.792-2.132), elevated body mass index ( HR = 1.397, 95% CI : 1.198-1.629), blood pressure ( HR = 1.284, 95% CI : 1.181-1.397), triglycerides ( HR = 1.171, 95% CI: 1.077-1.274) were independent risk factors, which promoted the elevated fasting blood glucose incidence risk in patients with fatty liver disease. Fatty liver combined with the above 2, 3, and 4 risk factors had apparently increased the incidence risk of elevated fasting blood glucose ( P < 0.001). Conclusion:People with fatty liver disease had a higher risk of elevated fasting blood glucose from the first year than those without. Age≥50 year’s old, elevated blood pressure, body mass index and triglyceride might increase risk of elevated fasting blood glucose in patients with fatty liver disease, combined with the above 2,3 or 4 risk factors can increase the risk of elevated fasting blood glucose.

At present, the most effective therapeutic method for end-stage liver fibrosis is liver transplantation. However, the application of liver transplantation is limited by a shortage of liver donors, a high incidence rate of surgical complications, graft-versus-host disease, and high medical costs. Umbilical cord mesenchymal stem cell (UC-MSC) transplantation may become a promising method for the treatment of liver diseases. UC-MSCs are adult stem cells which exhibit multipotential differentiation and can differentiate into hepatic parenchymal cells. Due to their functions including immune regulation and secretion of trophic factors, UC-MSCs can inhibit immune response, promote hepatocyte regeneration, alleviate the progression of liver fibrosis, and improve liver function. In addition, compared with bone marrow mesenchymal stem cells, UC-MSCs have abundant sources, noninvasive collection, and high safety and thus they are attracting more and more attention. This article reviews the characteristics of UC-MSCs and their mechanism of action in the treatment of liver fibrosis, as well as risks of UC-MSCs therapy.